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Cell Physiol Biochem. 2014;34(2):533-42. doi: 10.1159/000363020. Epub 2014 Aug 8.

Induction of myocardial PDCD4 in coronary microembolization-related cardiac dysfunction: evidence from a large-animal study.

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  • 1Department of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning, China.



Coronary microembolization (CME) has been linked to myocardial inflammation and apoptosis. This study aims to investigate the role of the apoptotic protein PDCD4 in the myocardium after CME in minipigs.


Seventy Bama minipigs were randomized into four groups: control, CME, CME plus PDCD4-siRNA and CME plus control siRNA. CME was induced by injecting polyethylene microspheres into the left anterior descending artery. Cardiac function was evaluated. HE and HBFP staining were used to observe the degree of infarction. Western blotting and qPCR were used to evaluate the expression of PDCD4, TNF-α and caspase-3. The measurements were performed at 0, 3, 6, 9, 12 and 24 h after CME modeling in the CME and control groups.


Cardiac function in the CME group was significantly decreased compared with the control group (P<0.05) and the expression of PDCD4 and TNF-α increased significantly (P<0.05). However, the infarct area did not differ between the CME and control groups at any time point (P>0.05). Furthermore, PDCD4-siRNA improved cardiac function and reduced PDCD4 and TNF-α expression compared with the CME plus control siRNA group at 9 h after modeling (P < 0.05), while the caspase-3 level was not different between the two groups.


PDCD4 induction may be involved in CME-related cardiac dysfunction, and PDCD4 inhibition via siRNA may attenuate the cardiac impairment and be used as a treatment strategy for CME.

© 2014 S. Karger AG, Basel.

[PubMed - indexed for MEDLINE]
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